Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors analyse the polymorphism of certain hereditary extrapyramidal system diseases and call attention to their intrafamilial and interfamilial characteristics. Various diseases are described: 5 forms of hepatolenticular degeneration, 2 forms of torsion dystonia, 3 forms of idiopathic tremor, 3 forms of Huntington's chorea. Clinical peculiarities, peculiarities of the course of the disease, and biochemical changes in these diseases are discussed. In the forms associated with rigidity or with hyperkinesis in the same disease (torsion dystonia, Huntington's chorea) abnormalities of various directions were discovered in the metabolism of neurotransmitters and amino acids, which make possible application of differentiated pathogenetic therapy.
Neurol Neurochir Pol
PMID:[Problems of the clinical polymorphism of hereditary extrapyramidal disorders]. 732 4

In a patient rhythmic, coarse tremor of the right hand and fingers 5/sec. was observed 5 weeks after severe craniocerebral injury. The tremor occurred at rest and increased during movements but disappeared in sleep. In view of associated mask-like facial expression, salivation, cog-wheel sign in the right upper extremity the diagnosis of traumatic, hemiparkinsonian syndrome was made and treatment with Nacom was started. Normal concentration of homovanilic acid in the cerebrospinal fluid and lack of effect of Nacom treatment failed to confirm this diagnosis. Nine weeks after trauma a rotatory movement of the right upper extremity appeared additionally. It is to be accepted that this was an involuntary movement poorly classificable which disappeared spontaneously.
Neurol Neurochir Pol 1980
PMID:[Transient involuntary movements after severe cranio-cerebral trauma]. 745 33

A minority of patients treated with serotonergic agents develop a fulminant and potentially life-threatening illness characterized by changes in mental status, restlessness, myoclonus, hyperreflexia, tremor, shivering, incoordination, hyperthermia, diaphoresis and diarrhea. This condition of serotonergic hyperstimulation is called the "serotonin syndrome". The author describes an adverse response in a patient given fluoxetine and lithium. A 61-year-old woman presented to casualty exhibits nearly all of the diagnostic criteria proposed by Sternbach [17].
Psychiatr Pol
PMID:[A case of serotonin syndrome]. 756 25

The effect of Thymomodulin-TFX on pentetrazole convulsions, tremorine-induced tremor, pain response to intraperitoneal acetic acid injection, hexobarbital sleeping time, isolated guinea pig ileum, isolated rat uterus, rabbit skeletal muscle response, diuresis and corneal response was tested. In addition the effect of TFX on reproduction of albino rats was investigated. In doses up to 20 mg/kg, 8 times higher than clinical doses, TFX did not reveal any unwanted effects. The results of tests widen the security margin for TFX's usage.
Acta Pol Pharm 1993
PMID:Pharmacological properties of the extract of thymus gland (Thymomodulin-TFX) and its effect on reproduction. 806 58

Fifty-five patients were treated with botulin injections into the muscles showing dystonia, contracture or tremor. Twenty two of them had torticollis, 21 had blepharospasm, 10 had hemifacial spasm, and 2 had tremor. In all, 112 injections were done with good result in 64%, slight effect in 27% and without effect in 9% of the cases. Similar results have been reported from other centers in the world. Adverse effects were not significant and disappeared after several days or weeks. They included ptosis, speech and deglutition disturbances, general weakness and neurotic reactions. These adverse effects developed in 12 cases. In cases of tremor the dose as well as the technique of injections must be individualized. The method is an important therapeutic advance and can be applied in outpatient clinics.
Neurol Neurochir Pol
PMID:[Own experience with botulinum treatment of dystonia]. 854 26

Clinical observations of 68 preterm and term newborns with ultrasonographically diagnosed PVL treated in the Infant Department of the Child Health Center in Warsaw from January 1985 to December 1990 are presented. The most frequent clinical sign in newborns was hypotonia of the lower extremities. Tremors were significantly more frequent in preterms. During the infant period, more clinical signs occurred in connection with cerebral atrophy (ventriculomegaly and subdural space enlargement). Observations were carried from the neonatal period to the age of 6 years. Development of 42 (61.8%) children was normal. In 26 (38.2%) infants from 6 to 12 months old, cerebral palsy (most frequently diplegia) was diagnosed. No significant differences in the frequency of cerebral palsy between terms and preterms were found. Epilepsy and minimal brain dysfunctions were also present.
Pediatr Pol 1996 Sep
PMID:[Estimate of clinical dynamic in periventricular leukomalacia]. 892 87

Pharmacological treatment of essential and symptomatic tremor is not satisfactory. Introduction of botulinum toxin (BTX) has brought a new approach to tremor treatment. BTX is injected into carpal flexors and extensors about 100 i.u. into each muscle, higher doses are injected into flexors and lower into extensors. Beneficial results are observed in 50 to 67% of the patients. The author treated 5 patients with tremor of various origin with good result in 3 cases (60%), but in all cases weakness of hand muscles and middle finger dropping were observed. BTX treatment is indicated in certain cases of hand disabled by tremor.
Neurol Neurochir Pol 1998
PMID:[Botulinum toxin in the treatment of tremor]. 960 53

Idiopathic Parkinson Disease accounts for approximately 75% of all cases of parkinsonism. The described case of Corticobasal Degeneration (CBD), until now not presented in Polish medical literature is a relatively rare example of so-called "parkinson plus" syndrome. The authors present the case of a 56 years old woman with asymmetric onset of rigidity and atypical tremor of upper extremity followed by gait disturbances (gait apraxia), dysarthria, bilateral pyramidal signs and myoclonus. Complete lack of clinical improvement after treatment with L-dopa and progressive character were observed from the onset of the disease. The presented case seems to be helpful in differential diagnosis of parkinson plus syndromes and specially CBD, which seems to be difficult in the first stages of the disease. Although the case was not neuropathologically verified (patient is still alive) the diagnosis seems to be almost true.
Neurol Neurochir Pol
PMID:[Cortico-basal degeneration. Diagnosis and differentiation and the description of the first case in Poland]. 1035 40

Clinical features were compared of a patient with the 48,XXYY karyotype and a case of 47,XXY/48,XXYY mosaicism. In the former patient tremor of the upper extremities of unclear aetiology was present. In both cases epilepsy was suspected. Similarly as in other cases of 48,XXYY karyotype the first patient had skeletal anomalies, abnormalities of dermatoglyphics and personality changes. These features are rarely found in Klinefelter syndrome. The differences in relation to the syndrome were less evident in the case of mosaicism 47,XXY/48,XXYY.
Neurol Neurochir Pol
PMID:[Neurological aspects of two patients with non-mosaic and mosaic polysomy of the X and Y chromosomes]. 1039 34

Degeneration of dopaminergic neurons that project from substantia nigra to striatum is the primary mechanism that causes Parkinson disease (PD). This death of dopaminergic cells disturbs control over impulses sent from the motor cortex and hence results in the presence of three cardinal motor signs: tremor, rigidity, bradykinesia. The cause of Parkinson disease is unknown. Current treatments relieve symptoms but do not halt the progression of the disease. It is not yet known what causes neurons to degenerate. Influences of aging, environmental toxins, genetic susceptibility have been pointed out by researchers, but the theory of oxidative stress seems to be the most convincing. It is supposed that SN neurons are exposed to oxidative reactions from dopamine metabolism (production) during which hydrogen peroxide and toxic semiquinones are formed. Additionally, in brains of PD patients there are decreased concentrations of defence mechanisms such as glutathion and compensatory ferritin that binds iron, maintaining it in its safe state (Fe2+ iron takes part in Fenton reaction that leads to free radicals production). However, we have to admit that Parkinson disease is probably multifactorial, and the combination of the above stated factors may cause the disease.
Neurol Neurochir Pol
PMID:[Factors which can play important role in pathogenesis of Parkinson disease]. 1061 5


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